{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE293nnn/GSE293902/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE293902"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Regulation of germinal center B-cell homeostasis by Deltex-1 (Dtx1) [scRNA]","description":"Germinal centers (GC) are sites for the clonal expansion and affinity maturation of B-cells that is coordinated by interaction with follicular dendritic cells (fDCs) and T follicular helper (TFH) cells. Loss of GC homeostasis can contribute to the development of B-cell malignancies and autoimmunity. Here we sought to investigate the GC-specific function of Deltex-1 (Dtx1), a gene that is highly expressed in GC B-cells and is a prominent target of aberrant somatic hypermutation. Dtx1 conditional knock-out (cKO) led to a competitive advantage in the GC reaction and marked GC hyperplasia accompanied by expansion of, and dependence upon, the fDC network. Dtx1 cKO GC B-cells bore transcriptional evidence of Notch and Myc pathway activation, and genetic inhibition of Notch activity led to resolution of GC hyperplasia. Together, these data implicate Dtx1 as a critical regulator of fDC-derived Notch signaling and GC homeostasis.","dates":{"publication":"2026/04/04"},"accession":"GSE293902","cross_references":{"GSM":["GSM8893184","GSM8893185","GSM8893186","GSM8893187","GSM8893188","GSM8893189","GSM8893190","GSM8893191"],"GPL":["24247"],"GSE":["293902"],"taxon":["Mus musculus"]}}